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. Author manuscript; available in PMC: 2022 Oct 1.
Published in final edited form as: Prog Biophys Mol Biol. 2021 May 12;165:3–7. doi: 10.1016/j.pbiomolbio.2021.05.002

Figure 1.

Figure 1

A) In non-cancerous cells, reactive oxygen species (ROS) exist at moderate to low levels to aid in the regulation of various cell signaling pathways. The DNA damage response (DDR) is capable of repairing oxidative stress-induced DNA damage and the integrity of the genome is maintained. B) Cancer cells have an increased amount of ROS, shifting the redox balance of the cell. The increased oxidative stress inflicts damage on the DNA of the cancer cell, contributing to cancer’s genomic instability. The DDR pathways, while activated from the ROS-induced DNA damage, are also hindered by the increased oxidative stress levels across the cancer cell. When anti-cancer therapy is applied to the cancer cell, the levels of ROS increase as a stress response. Both the ROS-induced and therapy-induced DNA damage activate the DDR; however, the DDR pathways are still hindered by oxidative stress and are not capable of repairing DNA at the rate it is being damaged.